Public Service Announcement: Calling all Low-carb, Low-fat and Veg*n advocates.

Cont'd from The cause of America's rising obesity rate is irrelevant. The cure for it is what's important.

While you're arguing about which arrangement of deckchairs on deck is best, the ship is sinking.

From https://twitter.com/MaxCRoser/status/936695363167313920

People are getting fatter and sicker in increasing numbers around the world, due to increasing numbers of people over-consuming over-refined, over-marketed & over-moreish Food Products. Getting people to change their diet back to one based on minimally-refined produce would be an improvement.

Why don't you agree to say the same thing, e.g.:-

Base your diet on whole, minimally-refined produce, rather than products. Tweak it to suit.

While you're wasting time shouting each other down, the Food Product Industry is laughing all the way to the bank.

Cont'd on Free will? It's just an illusion! How the Food Product Industry gets people to dance to their tune, part 1.

When bad science goes...pretty much the same!

After the previous post, you may have got the impression that things are getting worse. Hmmm!

From http://covermyfb.com/covers/27316/say%2Csee+and+hear+no+evil

Hat-tip to James Beckerman, MD for https://twitter.com/jamesbeckerman/status/507544419847786496, which refers to Comparison of Named Diet Programs Finds Little Difference in Weight Loss Outcomes.

This study comes to the opposite conclusion of the study in my previous blog post. As that study was a pile of poo, that must mean that this study is 100% correct, right? Hmmm!

Your enemy's enemy is not necessarily your friend. See What about the Other Weight Loss Diet Study??
"Previous meta-analyses, such as Hession et al, had balanced inclusion criteria that allow us to directly compare low-fat to low-carb diets.  They reported exactly what anyone would expect who is familiar with the weight loss diet literature:

1. At 6 months, low-carb diets consistently lead to greater weight loss than low-fat diets. 
2. At one year, the difference has all but disappeared. 
3. Neither diet produces particularly impressive weight loss at one year or more.
4. The weight loss effectiveness of typical low-fat diets tends to be modest at all time points.

Oh, well. It could have been a lot worse!
 

When good science goes bad, part n+1.

In When good science goes bad , I looked at the effect of funding bias on research.

From https://www.youtube.com/watch?v=sJ5jbxMjexo

Effects of Low-Carbohydrate and Low-Fat Diets: A Randomized Trial has just been published. As expected, low-carbers are positively creaming themselves over it. I instantly smelled a rat, as the full study was behind a pay-wall.

Remembering Krauss' shenanigans with "carbohydrate", consisting of 50% sugars + 50% "complex" carbs (maltodextrin & amylopectin are complex carbs that hydrolyse into glucose so rapidly that they have a GI of 100 on the "Glucose=100" scale.), I suspected dodgy carbs in the "Low-fat" group.

Luckily, David L. Katz, MD, MPH, FACPM, FACP had read the full study, and wrote about it in Diet Research, Stuck in the Stone Age.

As I suspected, it was another "fix-up" job, rigged to make low-carb diets look good, and low-fat diets look bad.

See also:-
Low-carbohydrate vs. Low-fat diets for Weight Loss: New Evidence,
What I Learned By Actually Reading That Low-Carb Is Best Study,
Is low-carb really the best weight loss diet? and
A Question about the latest diet study ...

Dear ItsTheWoo, how do you do?

This post is attacking what I consider to be faulty reasoning. It's not a personal attack on ItsTheWoo, who I like (even though she drives me up the wall, sometimes!).

From http://hypetrak.com/2011/10/mayer-hawthorne-how-do-you-do-full-album-stream/

See What I believe and what I don't.
The basic The Energy Balance Equation:- Change in body stores = E_in - E_out
For a detailed mathematical analysis of weight change, see Completing the trine: vive la différence!

From Back to black, CIAB, pharmaceutical drug deficiencies & nerds:-
Where body weight is concerned, calories count (but don't bother trying to count them).
Where body composition is concerned, partitioning counts.
Where health is concerned, macronutrient ratios, EFAs, minerals, vitamins & lifestyles count.


The faulty reasoning is in Dear Nigel and other CICO zealots: you are ignorant. Charming!

I'll quote passages from it and refute them, one by one.

• "With a zero caloric deficit, there is zero weight change"

"FACT: Calories neither determine weight OR body composition with certainty. Nigel / some CICO zealots may agree body composition changes are privy to nutrition, but wt is 100% controlled by calories. This is something they pretty much made up and biological science does not at all support this idea. Calories neither control body composition OR body weight/mass with any certainty. The bulk consumed with fork and spoon does not need to stick on your body in the form of a mass laden tissue, ever."
Calories determine weight change. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned). It would have been nice if Fig. 6 had contained a plot of "Effect of energy intake on change in body weight", but it didn't.
LBM = Lean Body Mass
FM = Fat Mass = Body Fat
Weight change = LBM change + FM change
Weight change varies from ~+3.5kg (@ +2,500kJ/d) to ~+9.1kg (@ +5,900kJ/d).
(Maximum weight increase)/(minimum weight increase) = 2.6
(Maximum kJ/day increase)/(minimum kJ/day increase) = 2.36
∴ A calorie IS a calorie (where weight change is concerned).
∴ Insufficient protein can result in loss of LBM (bad).

The main thrust of ItsTheWoo's argument is that inter-personal variations in weight gain from subject to subject, invalidates Bray's conclusion. It doesn't.
Some subjects become more energetic on a 40% caloric surplus, which increases their NEAT & TEA, which increases their Eout, which reduces their weight gain.
Some subjects don't change their energy on a 40% caloric surplus, which doesn't change their NEAT & TEA, which results in intermediate weight gain.
Some subjects become less energetic on a 40% caloric surplus, which decreases their NEAT & TEA, which decreases their Eout, which increases their weight gain.

I believe that the Insulin Sensitivity (IS) of the subject determines which category they fall into and by how much. The higher the IS, the higher the energy, as high IS results in low serum insulin, which minimises sedation. Energy Balance always applies.

I've never stated that Calories exactly determine weight change. That's a strawman.
I've never stated that Calories determine body composition. That's a strawman.

•  " Every subject [in bray's overfeeding study] gained weight (mostly fat mass) during the 40% energy excess overfeeding period. "

"Again, making crap up. There is NO RULE IN BIOLOGY which states all consumed energy must be retained as body mass. Indeed most typical people gain fat during overfeeding (with great resistance/inefficiency of fat gain), but it is indeed possible to hardly gain any or none at all as in constitutional thinness. What happens during calorie consumption among different people (and perhaps, different DIETS and different TIMES and different ENDOCRINE situations...) is a wild card determined by the biology i.e. neuroendocrine functions of the animal in question. There is NOTHING about physics which reflects / informs physiology other than the basic fact the latter exists within the former (which, again, tells us NOTHING ultimately). How organisms process consumed nutrition is not a physics question. There is no freakin' law of physics or physiology for that matter which states nom nom time = thigh chub. You don't have to wear that pizza as a popeye's muscle or as a shelf butt."
Somewhere within all of the irrelevant waffle about rules & laws, ItsTheWoo raises an interesting point. Although a caloric surplus is always required for weight gain, eating more Calories can sometimes result in zero weight gain. How so? From ItsTheWoo's link:-
"Conclusion: This data is the first to demonstrate a resistance to weight gain in constitutional thinness (CT) population in response to 4-week fat overfeeding, associated with an increase in resting energy expenditure and an emphasised anorexigenic hormonal profile.
In CT people, their energy expenditure increases in line with their energy intake. Therefore, even though they're eating more Calories, there's no caloric surplus, therefore there's no weight gain. Energy Balance always applies.

• "Yes, kcals do get wasted. You don't understand things quantitatively i.e. how many kcals get wasted."

"I know anxious/obsessional people like the safe feeling of balancing calories. The fact reality is more complex and you can't just enter things in a phone app and be ASSURED of what is going on in your body, doesn't invalidate the truth of the fact metabolic reactions are more complex THAN CALORIES.

Just because it is *impossible* for a reasonable free living human to quantify all of the metabolic, endocrine, nervous system factors influencing adipocyte growth changes does not mean they don't fucking exist."
ItsTheWoo left out my calculations. Here they are:-"if I eat 2000 calories of a ketogenic diet in 3 hrs, most of it is wasted as heat, physical energy (I know, because I am EXTREMELY warm/energetic) and then the rest of time i am using a relatively greater percent of stored fat."
Do you know at what rate you're burning-off extra energy intake as heat energy output when you're "EXTREMELY warm/energetic"? Here's an estimate:-
If the mean TEF for your meal is 11% (assuming your meal is 50%E protein & 50%E fat), that's 220kcals (921kJ) "wasted" as heat energy. That'll make you feel EXTREMELY warm, as 220kcal raises the temperature of 57kg of water (your body) by 3.84°C.

A 2,000kcal meal (a whole day's worth of food) takes a lot longer than 3 hours to digest & absorb. I'll guesstimate it as 24 hours. 921kJ of extra heat power over the course of 24 hours = 10.7W, which is an increase of 17.7% over your normal Metabolic Rate of ~60W heat power (~1kcal/minute).
It's easy to "prove" something by being vague. That's PSEUDOSCIENCE. I do science. If you do the maths, you can see that, of the 2,000kcal ketogenic meal, most of it isn't wasted as heat, because if most of it is wasted as heat, ItsTheWoo would spontaneously combust!

• "Dr. Robert C. Atkins made the same fundamental cock-up when he said that humans pissed-out loads of kcals of ketones each day, giving a Metabolic Advantage to ketogenic diets."

"1) The advantage of a ketogenic diet (non-fasting) does exist, so it's not a 'cock up", even if his mechanism was wrong.
2) If atkins was wrong (you pee out all LCHF food) who cares? That was 30+ years ago. He was a cardiologist who observed a VLC diet made him slim. He used his medical education to hypothesize a reason why. His hypothesis was wrong, but his observations were right. This happens all the time in science or basic human reasoning; make observations, form hypothesis. The hypothesis may be wrong, the findings are STILL RIGHT (i.e. low carb diets DO make slim, just not via peeing away ketones)."
1) There is no Metabolic Advantage to ketogenic diets. See https://www.jbc.org/content/92/3/679.full.pdf
2) Atkins' observations were wrong. See The Battle of the Diets: Is Anyone Winning (At Losing?)
a) Low-Carb diets work better than High-Carb diets for people who are Insulin Resistant.
b) Low-Carb diets work worse than High-Carb diets for people who are Insulin Sensitive.
c) Low-Carb diets work the same as High-Carb diets for everybody in Metabolic Ward Studies.
If there's a Metabolic Advantage to ketogenic diets, they would work better than high-carb diets all the time. They don't. See How low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes for my hypothesis, which explains a), b) and c).

Ketogenic Diets and Sudden Cardiac Death.

Last night, thanks to comments on my previous post, I stumbled across The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism, then a Google search led me to Sudden Cardiac Death and Free Fatty Acids.

The following graph is Figure 1 from Lack of suppression of circulating free fatty acids and hypercholesterolemia during weight loss on a high-fat, low-carbohydrate diet.

Nice Insulin, shame about the FFAs.

From the first link above:-
"Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins."

From the third link above:-
"Weight loss was similar between diets, but only the high-fat diet increased LDL-cholesterol concentrations. This effect was related to the lack of suppression of both fasting and 24-h FFAs."

See also Elevated plasma free fatty acids predict sudden cardiac death: a 6.85-year follow-up of 3315 patients after coronary angiography, and Circulating Nonesterified Fatty Acid Level as a Predictive Risk Factor for Sudden Death in the Population.

I think that's quite enough bad news for a Friday afternoon.


EDIT: So much for fat being a "clean-burning" fuel for the heart. Some people believe that, because dietary fats pass from the small intestine, via the Lacteals, to circulation at the Subclavian vein, this means that the heart prefers to burn fatty acids.

From Page 10 of HIGH CARBOHYDRATE DIETS: MALIGNED AND MISUNDERSTOOD:-

Human erythrocytes (red blood cells) contain cholesterol and it can contribute towards atherosclerosis. See https://twitter.com/Drlipid/status/496625195738619904.

See also Evidence for a cholesteryl ester donor activity of LDL particles during alimentary lipemia in normolipidemic subjects. This is more evidence that very high fat meals are atherogenic, which is relevant to Ultra-high-fat (~80%) diets: The good, the bad and the ugly.

Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base, by Richard D Feinman et al.

Another Bookmarking post.

From https://dgeneralist.blogspot.co.uk/2013/11/the-low-carb-high-fat-diet.html

The study in question is Dietary Carbohydrate restriction as the first approach in diabetes management. Critical review and evidence base. Here are my comments on the 12 points.

Point 1 is wrong. For ~85% of people who have T2DM, hyper*emia is the salient feature, where * = glucose, TG's, cholesterol, NEFAs, uric acid etc. For ~85% of people who have T2DM, it's a disease of chronic excess.

Ad lib LCHF diet → ↓ Blood glucose & ↓ fasting TG's, but ↑ PP TG's, ↑ LDL-C, ↑ LDL-P & ↑ NEFAs. See Postprandial lipoprotein clearance in type 2 diabetes: fenofibrate effects.
↑ PP TG's is associated with ↑ RR of CHD.
↑ LDL-P is associated with ↑ RR of CHD.
↑ NEFAs are associated with ↑ RR of Sudden Cardiac Death.

Point 2: So? T2DM is a disease of chronic excess. Chronic over-consumption was caused by Food Industry marketing, not carbohydrates.

Point 3 is wrong. A caloric deficit is essential, to reverse liver & pancreas ectopic fat accumulation. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Point 4 is misleading. Feinman doesn't distinguish between different types of carbohydrates. Starches, especially resistant starches (e.g. Amylose) are beneficial. See Point 11.

Point 5 is moot. Prof. Roy Taylor found that motivation determines adherence. Prof. Roy Taylor's PSMF was adhered to. See Point 3.

Point 6 is correct. Prof. Roy Taylor's PSMF is ~1g Protein/kg Bodyweight, some ω-6 & ω-3 EFAs & veggies for fibre. See Point 3.

Point 7 is misleading. Siri-Tarino et al gave a null result by including low fat studies, also a dairy fat study which had a RR < 1 for increasing intake. Chowdhury et al gave a null result, as some fats have a RR > 1 for increasing intake and some have a RR < 1 for increasing intake.

Point 8 is irrelevant. ↑ Dietary fat → ↑ 2-4 hour PP TG's. See Point 1.

Point 9 is partly correct. Microvascular, yes. Macrovascular, no. See Point 8.

Point 10 is mostly irrelevant. See Point 8.

Point 11 ignores results obtained with high-starch diets, where the starch contains a high proportion of Amylose. See Walter Kempner, MD – Founder of the Rice Diet and From Table to Able: Combating Disabling Diseases with Food.

Point 12 is misleading. The low-carbohydrate part is fine. It's the high-fat part that can cause problems. See Point 8.

Why do some people have trouble doing things in moderation?

This is related to my previous post.

From http://www.kindredcommunity.com/2013/01/xtreme-eating-awards-2013-extremism-running-amok-at-americas-restaurant-chains/

Some people take low-carbing to an extreme, 'cos if reducing carbohydrate intake has benefits, reducing it to zero must be better. Oy!


We're told that eating 5 portions of fruit and vegetables a day is good for us. One patient who was admitted to St George's with malnutrition, had been eating more than 50 portions of fruit and vegetables a day, 'cos if 5 portions of fruit and vegetables a day is good for us, 50 portions of fruit and vegetables a day must be better. Oy!


People who are taking the anti-clotting medication Warfarin need to maintain an accurate balance between their warfarin dose and their Vitamin K intake to keep their INR between 2 and 3, as warfarin antagonizes vitamin K₁ recycling, depleting active vitamin K₁.
"Between 2003 and 2004, the UK Committee on Safety of Medicines received several reports of increased INR and risk of haemorrhage in people taking warfarin and cranberry juice. Data establishing a causal relationship is still lacking, and a 2006 review found no cases of this interaction reported to the FDA; nevertheless, several authors have recommended that both doctors and patients be made aware of its possibility. The mechanism behind the interaction is still unclear." Here's a clue...

From Possible interaction between warfarin and cranberry juice (emphasis, mine):-
"After a chest infection (treated with cefalexin), a man in his 70s had a poor appetite for two weeks and ate next to nothing, taking only cranberry juice as well as his regular drugs (digoxin, phenytoin, and Warfarin). Six weeks after starting cranberry juice he had been admitted to hospital with an INR (international normalised ratio) > 50. Before, his control of INR had been stable. He died of a gastrointestinal and pericardial haemorrhage. He had not taken any over the counter preparations or herbal medicines, and he had been taking his drugs correctly." Cranberry juice contains no Vitamin K. Oy!

"The Committee on Safety of Medicines has received seven other reports through the yellow card reporting scheme about a possible interaction between warfarin and cranberry juice leading to changes in INR or bleeding. In four cases, the increase in INR or bleeding after patients had drunk cranberry juice was less dramatic. In two cases, INR was generally unstable, and in another case INR decreased. Limited information is available about whether patients complied with their treatment in these cases.

Cranberry juice (Vaccinium macrocarpon) is popular and is also used to prevent cystitis. Interaction with warfarin is biologically plausible, because cranberry juice contains antioxidants, including flavonoids, which are known to inhibit cytochrome P450 enzymes, and warfarin is predominantly metabolised by P450 CYP2C9. The constituents of different brands of cranberry juice may vary, and this might affect their potential for interacting with drugs. Whether the constituents of cranberry juice inhibit CYP2C9 and therefore the metabolism of warfarin or interact in another way needs further investigation. Until then, patients taking warfarin would be prudent to limit their intake of this drink." Oy!

So, one man's inadvertent (his doctor should have warned him about eating next to nothing while taking warfarin) dietary extremism resulted in his own death and the restricted intake of cranberry juice for everybody else taking warfarin. Oy. :-(


P.S. It's about time an alternative to warfarin was found. It's difficult to maintain an accurate balance between warfarin dose and Vitamin K intake.

Jumping through hoops, and my Blog List.

I'm seeing a curious thing. The VLC "camp" seems to be "jumping through hoops" to prove a point.

From http://davidbressler.com/2013/08/26/easier-harder/

From Neuron fuel and function (emphasis & formatting, mine):-
"Ketones and lactate do not drive reverse electron flow through complex I. Glucose can. Palmitate certainly can. What you want from a metabolic fuel depends on the remit of your cell types. Neurons within the brain preserve information by their continued existence.

This is best done by burning lactate or ketones. NOT glucose and, of course, not FFAs.

Anyone who claims that glucose is the preferred metabolic fuel of the brain has not though (sic) about what a neuron has to do and what an astrocyte actually does do. Or much about the electron transport chain."

Basically, glucose is bad mmm-kay. Also, anyone who claims that glucose is the preferred metabolic fuel of the brain is a dumb-ass. Damn our livers & kidneys churning out glucose! Are they trying to kill us?

∴ Carbohydrates are bad and must be avoided at all cost! This, of course, is utter nonsense.

Glucose can drive reverse electron flow through complex I. Can means that it's possible. Is it probable?

On a hypercaloric Western diet of excessive crap-in-a-bag/box/bottle, yes.

On a Kitavan diet of ~70%E from tubers, no.

On a diet of Basmati rice & beans, no.

On a diet of whole fruits, no.

See also Another crash and burn on low carb paleo and CrossFit. Enough of the 'carbs are evil' nonsense. Carbphobia is hurting a lot of people.

I have a list of blogs that I read on a regular basis. As a result of the bad science & cherry-picking displayed in various VLC blogs, I have deleted them from my Blog List.

See also Guest post: Denialism as Pseudoscientific Thinking.

How low & very low-carbohydrate diets don't work.

Having explained how low & very low-carbohydrate diets work, here are a few ways in which they don't work.

Uh, nope!

1. Hormonal clogs: This is a term used by Jonathan Bailor. I don't think he's referring to wooden shoes! The "clog", I'm guessing, is supposedly caused by that dastardly hormone insulin. Uh, nope!

See the following plots of RER vs exercise intensity after being on high-fat diet or low-fat diet.

RER = 0.7 ≡ 100%E from fat. RER ≥ 1.0 ≡ 100%E from carb.

The low-fat diet results in higher RER, so the body is burning a higher %E from carb and a lower %E from fat.

However, this doesn't make any difference to weight loss, as it's merely a substrate utilisation issue. In addition, when the body is burning a higher %E from carb, this depletes muscle glycogen stores faster, which lowers RER during the course of the exercise. So, it's not a problem.


2. Insulin: This is Gary Taubes' hypothesis. Insulin makes your body store carbohydrates as body fat. Uh, nope!

The only time that there's significant hepatic DNL is when there's chronic carbohydrate over-feeding. If you eat sensibly, there's no significant hepatic DNL.


3. A Calorie isn't a Calorie, where weight change is concerned: This is Richard D Feinman's hypothesis. "A calorie is a calorie" violates the second law of thermodynamics, therefore there's a metabolic advantage with low-carbohydrate diets. Uh, nope!

Where to start? Evelyn Kocur knows her Physics, so I'll start there. See The first law of thermodynamics (Part 1) and The first law of thermodynamics (Part 2).

From Second Law of Thermodynamics:-
"Living organisms are often mistakenly believed to defy the Second Law because they are able to increase their level of organization. To correct this misinterpretation, one must refer simply to the definition of systems and boundaries. A living organism is an open system, able to exchange both matter and energy with its environment."

People on ketogenic diets excrete very few kcals as ketone bodies. See STUDIES IN KETONE BODY EXCRETION (PDF). There is no significant Metabolic Advantage with low-carbohydrate diets.

How low & very low-carbohydrate diets result in more weight loss than high-carbohydrate diets for people with Insulin Resistance or Type 2 Diabetes.

See The Battle of the Diets: Is Anyone Winning (At Losing?) for trials where insulin resistant people lose more weight on low-carbohydrate diets than on high-carbohydrate diets and insulin sensitive people lose more weight on high-carbohydrate diets than on low-carbohydrate diets.

If Gary Taubes's carbohydrate/insulin hypothesis of obesity is correct, everyone would lose more weight on low-carbohydrate diets than on high-carbohydrate diets. This isn't the case, therefore Gary Taubes's hypothesis is not correct.

Although insulin is involved, it has nothing to do with "Hormonal clogs" or "Insulin fairies".

The Aragon Insulin Fairy

The Energy Balance Equation

Change in Body Stores = Energy in - Energy out, where... 

Energy in = Energy entering mouth - Energy exiting anus, and... 

Energy out = BMR/RMR + TEF + TEA + SPA/NEAT

See The Energy Balance Equation to find out what the above terms mean.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) have excessive insulin secretion in response to meals (postprandial hyperinsulinaemia). See Hyperinsulinaemia and Insulin Resistance - An Engineer's Perspective.

People with Insulin Resistance (IR), Impaired Glucose Tolerance (IGT) & Type 2 Diabetes (T2DM) also have impaired/no 1st phase insulin response to a sudden rise in blood glucose level. This introduces a time-lag into the negative feed-back (NFB) loop that regulates blood glucose level. If the input rise-time is less than the time-lag in a NFB loop, the output of the NFB loop overshoots. This is standard NFB loop behaviour. See Control of overshoot for more information.

1. On a high-refined-carbohydrate or high-GL diet, blood glucose level rises rapidly, with a rise-time that's less than the time-lag in the blood glucose regulation NFB loop. Insulin secretion from the pancreas overshoots in a positive direction. The resulting postprandial hyperinsulinaemia results in down-regulation of insulin receptors in the brain, which reduces insulin action in the brain. When the insulin level eventually falls to normal a few hours later, the brain interprets a normal insulin level as hypoinsulinaemia. Hypoinsulinaemia results in ravenous hunger, as insulin is a short-term satiety/satiation hormone in the brain (leptin is a long-term satiety/satiation hormone in the brain). Ravenous hunger results in over-eating. Energy in increases. Postprandial hyperinsulinaemia also results in postprandial sleepiness. Energy out decreases. ∴ Body stores increase. There are also accusations of gluttony & sloth!

2. On a low-carbohydrate or low-GL diet, there are small fluctuations in blood glucose & insulin levels. There is no ravenous hunger. There is much less/no over-eating. Energy in decreases. There is no massive postprandial hyperinsulinaemia. There is much less/no postprandial sleepiness. Energy out increases. ∴ Body stores decrease.

In addition, there is a loss of water weight due to a loss of liver & muscle glycogen. This can be ~2kg in one day (it varies from person to person). Kidneys can increase their output of urine for hormonal reasons. This can increase water weight loss to ~5kg. See Why counting Calories and weighing yourself regularly can be a waste of time.

There are also other hormones involved. For a Facebook discussion with James Krieger that led to the updating of this post, see https://www.facebook.com/james.krieger1/posts/10153228943648587

In Metabolic Ward studies, food intake is tightly controlled, so postprandial hunger doesn't result in over-eating. Energy expenditure is also controlled, so postprandial sleepiness doesn't significantly affect energy expenditure. This is why varying Fat:Carb ratios (with Protein held constant) makes no significant difference to weight in a Metabolic Ward. See Energy intake required to maintain body weight is not affected by wide variation in diet composition.

Inter-personal variations in postprandial hyperinsulinaemia, postprandial sleepiness & energy out explain the inter-personal variations in weight gain seen under hypercaloric conditions. See Bray et al shows that a calorie *is* a calorie (where weight change is concerned).

Insulin Resistance can be fixed. See Insulin Resistance: Solutions to problems.

Type 2 Diabetes can also be fixed. See Reversing type 2 diabetes, the lecture explaining T2D progression, and how to treat it.

Aim to fix the problem. If it's impossible to fix the problem, a low-carbohydrate diet as an adjunct to medication is fine.

I'm NOT a lipophobe, I'm a very naughty boy!

First, postprandial triglycerides again. From Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in Women, here's a plot of HR for future CHD vs TG's at various times after eating.

Hazard ratio (HR) and 95% confidence interval (CI) for highest vs lowest tertiles of triglyceride level (see Table 3 for values), adjusted for age, blood pressure, smoking, hormone use, levels of total and high-density lipoprotein cholesterol, diabetes mellitus, body mass index, and high-sensitivity C-reactive protein level.

Notice how the HR falls with increasing time from last meal. As TG's ≥12 hours after eating are a surrogate for Insulin Resistance (IR) and the HR is only 1.04 (95% CI 0.79 - 1.38), this strongly suggests that IR is not a significant factor.

It's been suggested that IR might increase PP TG's in the 2 - 4 hour period due to impaired clearance. According to Fig. 3B in Extended effects of evening meal carbohydrate-to-fat ratio on fasting and postprandial substrate metabolism, TG clearance in healthy men doesn't significantly start until after 4 hours has elapsed. Therefore, an impairment in TG clearance isn't going to make a significant difference to TG level in the 2 - 4 hour period.

Second, the reason why I'm having to repeat myself is due to Cholesterol: Do chylomicrons clog your arteries? (2), where I've been called "my resident lipophobe". As I drink Gold Top milk (5.2g of fat/100mL) and eat pork including belly slices (you know, those strips of pork with a lot of fat on them), I'm being attacked for something that I'm not.

What I'm criticising is dietary extremism. Eating fats in foods is fine by me, but eating sticks of Kerrygold butter and/or dumping loads of butter and/or MCT oil into coffee to achieve "Nutritional Ketosis" is not a good idea. Anyway, here's an amusing spoof on Bulletproof coffee.

Defending the indefensible: Gary Taubes and *that* statement about gluttony.

Here's another "video" (it has sound and static images only). As I haven't learned how to embed a YouTube video that starts at a specific time, here's a link to it and a picture of it:- Gary Taubes' "Why We Get Fat" IMS Lecture On August 12, 2010 (Part 8 of 8), starting at 8 minutes and 13 seconds in.

To quote: "You can basically exercise as much gluttony as you want, as long as you're eating fat and protein."

Itsthewoo told me that Taubes was being ironic i.e. he was joking. I call bull-shit on that, for the following reasons.

1) You don't joke about something as important as diet, in a video that's likely to be heard by many people.

2) If you are foolish enough to joke about something as important as diet, you make 100% certain that listeners know that you're joking, by stating in the very next sentence that the preceding sentence was a joke. Taubes didn't do that.

3) I didn't hear chortling or any other audible clue that Taubes was joking. Did you?

I therefore conclude that itsthewoo is hearing (and seeing) the world through "cognitive bias" Weird Filters , resulting in her hearing what she wants to hear. Sorry!

Not exactly rocket science, is it? Part 2

If there is a deficiency in "X", taking supplement "X" will correct the deficiency in "X".
∴ If problem "Y" is caused by a deficiency in "X", taking supplement "X" will fix problem "Y".

If there's no deficiency in "X", taking supplement "X" won't make any difference.
∴ If problem "Y" isn't caused by a deficiency in "X", taking supplement "X" won't fix problem "Y".

If a person spends a lot of time outdoors in skimpy clothing in sun that's higher than 45deg in the sky, it's highly likely that they won't be deficient in Vitamin D3. Therefore, supplementing with 5,000iu/day of Vitamin D3 won't highly likely do anything.

∴ If the above sun-worshipping person has type 2 diabetes, supplementing with 5,000iu/day of Vitamin D3 won't highly likely make any difference.

Not exactly...

Rocket Science!

There will be some people for whom all of the supplements & exercises that I recommend don't make any difference to their type 2 diabetes. Sorry about that. A low-carb (but not very-low-carb) diet will minimise your serum glucose level fluctuations without increasing your serum NEFA level excessively. See The problem with Diabetes.

Ketogenic diets - when they're not ketogenic.

High in the Arctic, Eskimo!

It's generally assumed that eating less than 50g/day of carbohydrate results in ketosis. Assume makes an ass out of "u" and "me". From Lyle McDonald's book The Ketogenic Diet:-

The Ketogenic Ratio (KR) = K/AK, where K = Ketogenic stuff and AK = Anti-ketogenic stuff.

K/AK =  (0.9*Fat + 0.46*Protein)/(1.0*Carbohydrate + 0.1*Fat + 0.58*Protein) where Fat, Protein & Carbohydrate are in grams.

For the treatment of epilepsy (very strongly ketogenic), K/AK must be greater than 1.5. For people who want to get into benign dietary ketosis, K/AK can be lower.

Eskimos eat a diet containing virtually zero dietary carbohydrate (~50g/day as muscle & liver glycogen). However, they are not in ketosis. See STUDIES ON THE METABOLISM OF ESKIMOS.

Eskimos eat so much protein that the Anti-ketogenic effect of Protein offsets the Ketogenic effect of Fat + Protein. Table IV is interesting, as it shows how much energy is lost as ketones on the third day of successive fasts in non-Eskimos (Subject #1 fasted once only). Note:- Beta-hydroxybutyric acid  produces 5kcals/g.

Subject #1:- 10.5kcals. ?kcals, ?kcals.
Subject #2:- 100.5kcals, 7.0kcals, 2.75kcals.
Subject #3:-  9.75kcals, 0.0kcals, 0.0kcals.

The answer is "not a lot" (except for Subject #2 on the first fast).

Continued on Ketogenic diets - when they're not ketogenic, Part 2.

Low-glycaemic diet seen to reverse diastolic dysfunction of diabetes.

From http://www.medscape.com/viewarticle/802947?nlid=30763_1301&src=wnl_edit_dail (Medscape log-in required):-

"Of 32 overweight or obese diabetic patients (mean body-mass index, 34) without cardiac disease who were engaged in a "rehabilitation program in order to lose weight" that included two hours of supervised aerobic exercise per day, half followed a low-glycemic diet (25% carbohydrate, 45% fat, 30% protein) and the other half a low-fat diet (55% carbohydrate, 25% fat, and 20% protein) for three weeks. The diets provided the same amount of calories. Those on the low-fat diet then switched to the low-glycemic diet for an additional two weeks"

"....the two diets led to about the same declines in weight and waist circumference..."

The diet was 25% carbohydrate, 45% fat, 30% protein.
It was a low-carbohydrate/low-glycaemic load diet.
It was not a very-low-carb diet.

Dr. Richard K Bernstein on insulin for type 2 diabetics, and some definitions.

Dr. Richard K Bernstein:-

Dr. Richard Bernstein, the world's leading low-carb diabetologist, says in Diabetes: The Basics:-
"Many people (including the parents of diabetic children) view having to use insulin as a last straw, a final admission that they are (or their child is) a diabetic and seriously ill. Therefore they will try anything else - including things that will burn out their remaining beta cells - before using insulin. Many people in our culture have the notion that you cannot be well if you are using medication. This is nonsense, but some patients are so convinced that they must do things the “natural” way that I practically have to beg them to use insulin, which is as “natural” as one can go. In reality, nothing could be more natural. Diabetics who still have beta cell function left may well be carrying their own cure around with them - provided they don’t burn it out with high blood sugars and the refusal to use insulin."

Some definitions:-

From Low-carbohydrate diet:-
"The term "low-carbohydrate diet" is generally applied to diets that restrict carbohydrates to less than 20% of caloric intake, but can also refer to diets that simply restrict or limit carbohydrates."
A typical woman consumes ~2000kcals/day. A typical man consumes ~2,500kcals/day. Therefore...

Very-low-carb diet = <10% energy from carbs ≡ <~50 or ~62.5g carbs/day.
Low-carb diet = <20% energy from carbs ≡ <~100 or ~125g carbs/day.
"Healthy eating" = >55% energy from carbs ≡ >~275 or ~344g carbs/day.

Not exactly rocket science, is it?

If Paul (astrophysicist) Jaminet met Jack (neurosurgeon) Kruse ;-)

The paleo diet was recently ridiculed as a food fad in Natural’s Not In It. It also came last in a US News Best Diets survey.

Ways of eating such as very-low-carbohydrate, low-carbohydrate, low-reward, paleo, primal, ancestral, just eat real food etc discourage the consumption of manufactured food products and encourage the consumption of produce. If a large percentage of the population stop filling their shopping baskets with manufactured food products and start filling them with produce, who suffers? Not exactly...

This is why the food manufacturing industry tries to ensure that the population gets the best nutritional and dietetic advice that money can buy. See also New study: Big Food’s ties to Registered Dietitians.

While libertarians and anarchists moan about freedom from government interference, the food manufacturing industry has the freedom to crap all over the aforementioned diets and influence people to buy manufactured food products. Morbidity is also very profitable for healthcare and drug companies.

I think that I've now flogged this particular horse to death!

A comment, a simile and insanity.

1) The comment: I'm just about to leave the following comment on Peter (Hyperlipid)'s blog post Insulin and the Rewards of overfeeding. I thought that it was so good at summing-up, I'll post it here first!
"All,

Insulin increases the amount of glucose & FFAs entering fat cells, muscle cells & the liver.

Insulin decreases the amount of glycerol & FFAs exiting fat cells & the amount of glucose exiting the liver.

Hyperinsulinaemia (which can produce sedation) results when one or more of the following tissues loses insulin sensitivity:- fat cells, muscle cells & the liver.

So, why do people keep saying that hyperinsulinaemia locks nutrients away in fat cells only, thus robbing other cells of nutrients, thus causing lethargy?

The relative insulin sensitivity of tissues determines the relative partitioning of nutrients into those tissues.

When tissues lose sensitivity to insulin, blood glucose control becomes impaired. This results in roller-coaster blood glucose levels after eating high-glycaemic carbohydrates. A rapidly-falling blood glucose level causes ravenous hunger. I have experienced this during medically-monitored tests (OGTTs & an insulin shock test).

Low-carb/ketogenic diets don't result in a roller-coaster blood glucose level and therefore don't cause ravenous hunger. Simples!

Overeating due to ravenous hunger is NOT gluttony, just as under-moving due to sedation is NOT sloth.

THIS is gluttony."

EDIT: This didn't go in my comment but should have:- "Low-carb/ketogenic diets result in the avoidance of moreish & calorific foods such as sweets, chocolate, cake, biscuits, pizza, Pringles etc. A single bite of such foods has a negligible effect on blood glucose & insulin levels, but encourages another bite and another and another ad nauseam, due to Food Reward.


2) The simile: I use similes. I used the simile "As happy as a pig in shit" in a comment somewhere on Woos blog. Now, you may (or may not) have noticed that my user-name is Nigeepoo. We Brits are obsessed by two things - The weather and our bowel movements. I find things to do with poo and farting amusing (schoolboy humour, I know!). I used the simile "As happy as a pig in shit" because it is amusing.


3) The insanity: According to Woo in the following comment:-
"Re: the comment...Sorry, not convinced.
You are basically refusing to admit your choice of words implied moral judgement. The phrase "happier than a pig in shit" is always applied to examples of people being content in immorality/bad behavior particularly gluttony and sloth... unless it is used ironically. Only an autistic or a non-english speaker would believe this crap."

Woo, you are as mad as a March hare. IMO of course, like everything I write. Duh!

It's all in a day's work (as measured in Joules)

Firstly, a relevant video by Flanders and Swann.


The title of this blog post is from the "Physics Man" sketch on The Now Show. Work (also heat) is another word for energy and there are two different units for it.

The calorie (cal) is the amount of energy required to heat 1g of water by 1°C. This is a tiny amount of energy. The dietary Calorie (Cal) = 1,000cal = 1kcal.

The Joule (J) is the SI unit of energy. 1J = 1kg*m^2/s^2.
1Joule/sec = 1Watt (W).

1kcal = 4.186kJ.

At rest, an average human body uses ~1kcal/min = ~4,186J/min = ~69.8J/sec = ~69.8W.

The brain uses ~5g of glucose/hour = 18.75kcal/hour (1g of carb = 3.75kcals, usually rounded-up to 4) = 78487.5J/hour = ~21.8W.

The heart uses ~10W. The liver, kidneys, gut and lungs run continuously so they use energy all of the time.

Skeletal muscle uses a variable amount of energy using a variable proportion of fuels, depending on what you're doing with it. A chap called Steve sent me a spreadsheet of results in 2004 when he underwent a metabolic test on a stationary bike while breathing through a respiratory gas analyser, which calculated kcals oxidised and fuel utilisation by measuring Respiratory Exchange Ratio (RER).

At 1kcal/min (resting), he oxidised ~95% from fat (~0.11g/min), ~5% from carb (~0.01g/min).
At 2kcal/min (12% max), he oxidised 100% from fat (0.22g/min), 0% from carb (0.00g/min).
At 3kcal/min (18% max), he oxidised 100% from fat (0.33g/min), 0% from carb (0.00g/min).
At 4kcal/min (24% max), he oxidised 99% from fat (0.44g/min), 1% from carb (0.01g/min).
At 5kcal/min (29% max), he oxidised 48% from fat (0.27g/min), 52% from carb (0.69g/min).
At 6kcal/min (35% max), he oxidised 62% from fat (0.41g/min), 38% from carb (0.61g/min).
At 7kcal/min (41% max), he oxidised 58% from fat (0.45g/min), 42% from carb (0.78g/min).
At 8kcal/min (47% max), he oxidised 46% from fat (0.41g/min), 54% from carb (1.15g/min).
At 9kcal/min (53% max), he oxidised 42% from fat (0.53g/min), 58% from carb (1.39g/min).
At 10kcal/min (59% max), he oxidised 44% from fat (0.49g/min), 56% from carb (1.49g/min).
At 11kcal/min (65% max), he oxidised 38% from fat (0.46g/min), 62% from carb (1.82g/min).
At 12kcal/min (71% max), he oxidised 41% from fat (0.55g/min), 59% from carb (1.89g/min).
At 13kcal/min (76% max), he oxidised 37% from fat (0.53g/min), 63% from carb (2.18g/min).
At 14kcal/min (82% max), he oxidised 30% from fat (0.47g/min), 70% from carb (2.61g/min).
At 15kcal/min (88% max), he oxidised 14% from fat (0.23g/min), 86% from carb (3.44g/min).
At 16kcal/min (94% max), he oxidised 0% from fat (0.00g/min), 100% from carb (4.27g/min).
At 17kcal/min (100% max), he oxidised 0% from fat (0.00g/min), 100% from carb (4.53g/min).

There are some interesting points about Steve's data:

1. Over a wide range of exercise intensities, the number of grams of fat Steve oxidised/min was fairly constant.

2. Up to 24% of maximum exercise intensity, Steve derived almost 100% of his energy from the oxidation of fat. Steve was on a LC diet, which shifts fuel usage away from carb and towards fat. This is known as "fat-adaptation".

3. Despite fat-adaptation, above about 45% of maximum exercise intensity, Steve derived more energy from the oxidation of carb than the oxidation of fat.

4. Despite fat-adaptation, above about 80% of maximum exercise intensity, Steve derived almost all of his energy from the oxidation of carb rather than the oxidation of fat.


Note that 17kcals/min = 1186.6W, or 1.19kW! Steve was aerobically fit. A less aerobically fit person derives a higher % of energy from the oxidation of carb than an aerobically fit person. This level of exercise intensity can be maintained for a few seconds only, as carb is oxidised both aerobically and anaerobically, which exhausts PhosphoCreatine stores in muscles and also causes an accumulation of lactate in muscles.

Muscle mass is very metabolically-active compared to fat mass, as one pound of fat mass oxidises only about 2kcal a day. See also Dissecting the Energy Needs of the Body – Research Review

See also It's all in a day's work (as measured in Joules) Part 2.


Here's another Physics Man.

We are not all the same.

Cont'd from Everyone is Different.

Lyle (McDonald) brought the following study to my attention to illustrate that "We are not all the same":- Some Metabolic Changes Induced by Low Carbohydrate Diets. On a very-low-carb diet, one subject’s total cholesterol rose to 12.9mmol/L (500mg/dL in US units). The others didn't.
See also LDL cholesterol goes sky high on fatty diet.

I posted the study in various blogs to make the above point. Here are some of the replies I got:-
"Lyle? Lyle McDonald? Is that where you got that study, Nigel?" and... "I’m usually a pretty polite guy, Nigel. But based on this quote from the beginning of the study you mentioned, the people who wrote this study were a bunch of f**kwads, and really don’t deserve our attention. It’s a hatchet job."
"That was a weird study (1967) what I could make of it." and... "The men did all the stages but the women only did 3 stages of the diet."
"The fats were mostly omega-6 PUFA 13-35 grams worth..."
"The report you cite is so old and out of date that it makes me cry..."

My point was well & truly missed. I got the distinct impression that people thought I was criticising very-low-carb, high-fat diets. I wasn't. The simple fact is that there is no "One True Diet" that suits absolutely everybody. In the olden days everywhere & in poor countries nowadays, people that ate/eat the wrong diet for their body died/die young. Nowadays in rich countries, they get put on drugs e.g. oral hypoglycaemics (to lower blood glucose) & hypolipidaemics (to lower blood cholesterol/triglycerides).

Please note that omega-6 PUFAs tend to lower serum cholesterol rather than raise it, as per Figure. 1 below from Individual fatty acid effects on plasma lipids and lipoproteins: human studies.

However, don't rush off and eat shed-loads of omega-6 PUFA (e.g. corn oil) in the mistaken belief that it will make you live any longer.

Cont'd on Everyone is Different, Part 2.